Gonadotropin-releasing hormone antagonists attenuate estrogen/progesterone-induced hyperprolactinemia in monkeys

Olive, David L.; Sabella, Vicente; Riehl, Robert M.; Schenken, Robert S.; Moreno, Arturo

doi:10.1016/s0015-0282(16)60740-9

Cited by 11 publications

(4 citation statements)

References 23 publications

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“…It has repeatedly been shown that peripheral injection of GnRH increases plasma PRL concentrations in adult rats ( 122 – 124 ), mice, hamsters ( 125 ), monkeys ( 126 ) and humans ( 127 – 133 ). Endogenous GnRH seems to exert a similar effect since treatment of castrated female monkeys with a GnRH antagonist causes PRL plasma concentrations to drop ( 126 , 134 ) and hyperprolactinemia induced by oestrogen/progesterone treatment is attenuated by administration of a GnRH antagonist ( 135 ). Also in female rats, blockade of endogenous GnRH by injection of anti-GnRH antiserum causes hypoprolactinemia ( 136 ).…”

Section: Gonadotrophs Signal To Lactotrophs Somatotrophs and Corticomentioning

confidence: 99%

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Denef

2007

J Neuroendocrinology

214

238

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Living organisms represent, in essence, dynamic interactions of high complexity between membrane‐separated compartments that cannot exist on their own, but reach behaviour in co‐ordination. In multicellular organisms, there must be communication and co‐ordination between individual cells and cell groups to achieve appropriate behaviour of the system. Depending on the mode of signal transportation and the target, intercellular communication is neuronal, hormonal, paracrine or juxtacrine. Cell signalling can also be self‐targeting or autocrine. Although the notion of paracrine and autocrine signalling was already suggested more than 100 years ago, it is only during the last 30 years that these mechanisms have been characterised. In the anterior pituitary, paracrine communication and autocrine loops that operate during fetal and postnatal development in mammals and lower vertebrates have been shown in all hormonal cell types and in folliculo‐stellate cells. More than 100 compounds have been identified that have, or may have, paracrine or autocrine actions. They include the neurotransmitters acetylcholine and γ‐aminobutyric acid, peptides such as vasoactive intestinal peptide, galanin, endothelins, calcitonin, neuromedin B and melanocortins, growth factors of the epidermal growth factor, fibroblast growth factor, nerve growth factor and transforming growth factor‐β families, cytokines, tissue factors such as annexin‐1 and follistatin, hormones, nitric oxide, purines, retinoids and fatty acid derivatives. In addition, connective tissue cells, endothelial cells and vascular pericytes may influence paracrinicity by delivering growth factors, cytokines, heparan sulphate proteoglycans and proteases. Basement membranes may influence paracrine signalling through the binding of signalling molecules to heparan sulphate proteoglycans. Paracrine/autocrine actions are highly context‐dependent. They are turned on/off when hormonal outputs need to be adapted to changing demands of the organism, such as during reproduction, stress, inflammation, starvation and circadian rhythms. Specificity and selectivity in autocrine/paracrine interactions may rely on microanatomical specialisations, functional compartmentalisation in receptor–ligand distribution and the non‐equilibrium dynamics of the receptor–ligand interactions in the loops.

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Section: Gonadotrophs Signal To Lactotrophs Somatotrophs and Corticomentioning

confidence: 99%

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Denef

2007

J Neuroendocrinology

214

238

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“…The physiological significance of the paracrine regulation of prolactin secretion by gonadotrophs is unknown. However, it probably operates in vivo, since GnRH has been reported to release prolactin in monkeys (609,1350) and in women during the menstrual cycle (295,1910).…”

Section: B) Autocrine and Paracrine Regulators Of Prolactin Se-mentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

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“…Endogenous GnRH seems to exert a similar effect since treatment of castrated female monkeys with a GnRH antagonist causes PRL plasma concentrations to drop (126, 134) and hyperprolactinemia induced by oestrogen/progesterone treatment is attenuated by administration of a GnRH antagonist (135). Also in female rats, blockade of endogenous GnRH by injection of anti-GnRH antiserum causes hypoprolactinemia (136).…”

Section: Gonadotrophs Signal To Lactotrophs Somatotrophs and Corticomentioning

confidence: 99%

Endogenous Cannabinoids: Structure and Metabolism

Bisogno

2008

J Neuroendocrinology

144

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D9 -Tetrahydrocannabinol (THC), the main psychoactive compound extracted from Cannabis sativa, is the most representative component of the mixture of therapeutic substances that are communally referred to as cannabinoids (1). It acts as an agonist at specific G-protein-coupled receptors, cannabinoid receptor subtypes CB 1 and CB 2 (2). The discovery of cannabinoid receptors has driven the investigation of the existence of their natural ligands and, soon after, endocannabinoids were identified. N-arachidonoyl-ethanolamine (AEA, anandamide) and 2-arachidonoyl glycerol (2-AG) are the two most studied endocannabinoids. They are biosynthesised 'on demand' by cleavage of their membrane lipid precursors N-arachidonoyl-phosphatidylethanolamine (N-ArPE) and sn-1-acyl-2-arachidonoylglycerols (DAGs) respectively, and then inactivated by intracellular hydrolysing enzymes. Cannabinoid receptors, endocannabinoids and enzymes that biosynthesise [N-acyl-phosphatidylethanolamine-selective phospholipase D (NAPE-PLD) and diacylglycerol lipase (DAGL)] and degrade [fatty acid amide hydrolase (FAAH) and the monoacylglycerol lipases (MAGL)] AEA and 2-AG, respectively, are key components in the endocannabinoid system (3). Despite a large number of excellent studies having contributed to the current understanding of the endocannabinoid regulation and function, further efforts are necessary to fully comprehend this signalling system. Here, a review on the current knowledge on structure and metabolism of the best studied endogenous cannabinoids is presented. In particular, this review concentrates on the mechanisms responsible for the biosynthesis and inactivation of the endocannabinoids, as well as on the several inhibitors of their metabolism identified to date. Endocannabinoids and related N-acyl-ethanolaminesEndocannabinoids are defined as endogenous compounds capable of binding to and functionally activating cannabinoid receptors. At least five endocannabinoids have been identified to date (Fig. 1). Anandamide, the amide between arachidonic acid and ethanolamine, was the first endogenous ligand to be reported at the end of 1992 (4) and additional polyunsaturated ethanolamines that bind to cannabinoid receptors, homolinolenylethanolamide and docosatetraenylethanolamide, have been isolated in the brain. Other endocannabinoids, all derived from arachidonic acid, were identified. The identification of 2-AG, the ester of arachidonic acid with glycerol, isolated from canine gut and brain has also been reported (5, 6). Subsequently, the first endocannabinoid characterised by ether bond, 2-arachidonyl glyceryl ether or noladin ether, was isolated from porcine brain (7) and N-arachidonoyldopamine (NADA), a selective CB 1 agonist and a potent agonist of vanilloid receptors, was discovered (8, 9). O-arachidonoylethanolamine, the ester derivative of ethanolamine with arachidonic acid, with the same molecular weight as anandamide but with opposite orientation of the polar ethanolamine moiety, was named virodhamine from the Sanskrit word virodha, ...

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Gonadotropin-releasing hormone antagonists attenuate estrogen/progesterone-induced hyperprolactinemia in monkeys

Cited by 11 publications

References 23 publications

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Endogenous Cannabinoids: Structure and Metabolism

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